The clinical detection of ischemia—an insufficient delivery of oxygen to meet a tissue's metabolic needs—is unreliable. Ischemia is especially difficult to detect when the ischemia is due to a localized interruption of blood flow—such as during a heart attack or stroke. Existing laboratory tests for ischemia, such as serum enzyme-leakage tests (e.g., for tests for cardiac isoenzymes after a heart attack) or EKG electrical tests, are insensitive indicators of such local tissue ischemia, especially during the early stages. Similarly, blood tests are also insensitive to local ischemia, as the ischemia is a result of low oxygenation in a local tissue, which is reflected in the local capillary oxygenation, not in the oxygenation of the arterial or venous blood when measured in the large central arteries and veins. Noninvasive imaging of ischemia lacks the immediacy that allows for early intervention or real-time feedback to other devices such as pacemakers.
Non-implantable ischemia sensors are known. For example, U.S. Pat. No. 6,532,381 teaches the detection of ischemia using externally measured electrical (EKG) monitoring and microprocessor control. However, such devices monitoring multiple external sites using wire leads placed upon the chest wall are not designed for implantability, which requires that issues of size, power consumption, biocompatibility, and robustness over time be optimized alongside sensing performance, a non-trivial task.
Implantable sensors are also well known. However, implantable sensors designed to detect ischemia are rare in the art, and none of these detect tissue ischemia directly. For example, U.S. Pat. No. 5,135,004, US Appn 2004/0122478, and WO 00/64534 predict the presence of ischemia based upon the electrical (EKG), blood pressure, local pH, and/or physical (acceleration during contraction) characteristics of the heart, while U.S. Pat. No. 6,527,729 discloses an implantable acoustic sensor that responds to heart failure by changes in the sound of the heartbeat. Further, U.S. Pat. No. 5,199,428 and US Appn 2004/0220460 teach implantable devices to monitor blood oxygenation (venous blood and arterial blood, respectively), in the latter case specifically rejecting local tissue saturation from encapsulation, thus teaching away from direct tissue monitoring. For reasons to be outlined in more detail later, such non-tissue blood oxygenation (whether arterial or venous) is insensitive to tissue ischemia, and is at best an indirect measure of tissue ischemia. For each of the devices above, then, ischemia is measured only by indirect and unreliable indicators of ischemia, such as by indicators of cardiac electrical, mechanical, and acoustic dysfunction. Another point to consider is that organs other than the heart are frequent sites of ischemia (such as in the kidney, liver, or gut), and the prior art is not directed to these other organs at all. Therefore, none of the above devices detect local tissue ischemia directly, nor can they be applied generally to any organ without regard to site.
All of the above devices are limited by being either non-implantable, by being at best an indirect measures of local tissue ischemia, or by being restricted to use in just one organ such as the heart due to the indirect measures of ischemia (such as sound or movement) which they employ.
None of the prior devices or methods allow for a direct detection of local tissue ischemia in a broad array of target sites using a long-term or short-term implantable system sensitive to local ischemia,
Such a system has not been previously described, nor successfully commercialized.